Location: Sugarbeet and Potato Research
Title: CIPC and 1,4-Dimethylnaphthalene Inhibit Sprout Growth Through Different Mechanisms and Do Not Extend Tuber Dormancy Authors
|Campbell, Michael -|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: March 26, 2010
Publication Date: August 15, 2010
Citation: Suttle, J.C., Campbell, M.A. 2010. CIPC and 1,4-Dimethylnaphthalene inhibit sprout growth through different mechanisms and do not extend tuber dormancy [abstract.] Potato Association of America. Abstract 118. p.122. Technical Abstract: Chlorpropham (CIPC) and 1,4-dimethylnaphthalene (DMN) are sprout inhibitors used to control sprouting in commercial potato storages. CIPC interferes with microtubule function and is thought to suppress sprouting by inhibiting cell division. DMN is a natural product produced by potato tubers whose sprout inhibiting abilities were first reported by Meigh et al. (1973). The mechanism of action of DMN is uncertain but it has been proposed to act by extending the natural period of tuber dormancy. This hypothesis was tested at both the physiological and molecular levels by comparing the effects of CIPC and DMN on hormone content and gene expression in relation to those found in both dormant and non-dormant tuber meristems. The endogenous contents of abscisic acid (ABA) in tuber meristems declined by over 75% during dormancy progression. The ABA content of meristems isolated from both CIPC and DMN-treated tubers declined to a comparable extent and was indistinguishable from meristems isolated from non-dormant tubers. The transcriptional profiles of the tuber meristems were distinct with over 5,000 genes exhibiting significant differences between the four samples. Although there were some similarities in the transcript profiles of CIPC- and DMN-treated meristems, the overall transcript profiles differed significantly which indicated differing modes of action of the two inhibitors. Importantly, there were significant differences in transcript profiles between CIPC- and DMN-treated meristems and those of dormant meristems. These results do not support the hypothesis that DMN acts by extending the natural period of dormancy and they suggest that CIPC and DMN inhibit sprouting through different mechanisms.